普罗布考联合胰激肽原酶对老年糖尿病周围神经病变患者氧化应激反应及血清NSE水平的影响

目的:探讨普罗布考联合胰激肽原酶对老年糖尿病周围神经病变患者氧化应激反应及血清神经元特异性烯醇化酶(NSE)水平的影响。方法:选择2015年8月至2017年8月我院接诊的94例老年糖尿病周围神经病变患者作为本研究对象,通过随机数表法将其分为观察组(n=47)和对照组(n=47)。对照组在常规治疗基础上给予胰激肽原酶治疗,观察组在对照组基础上联合普罗布考治疗,两组均连续治疗12周。比较两组治疗后的临床疗效、治疗前后运动传导速度(MNCV)、感觉传导速度(SNCV)、多伦多临床评分系统(TCSS)评分、血清丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)及NSE水平的变化和不良反应的发生情况。结果:治疗后,观察组临床疗效总有效率为93.62%(44/47),明显高于对照组[70.21%(33/47)](P0.05);两组正中神经、腓总神经MNCV、SNCV较治疗前均显著延长(P0.05),且观察组正中神经、腓总神经MNCV、SNCV均明显高于对照组(P0.05);两组TCSS评分各内容和总分、血清MDA、NSE水平较治疗前均显著降低(P0.05),且观察组TCSS评分中症状评分、反射评分、感觉评分和总分及、血清MDA、NSE水平均明显低于对照组(P0.05);两组血清超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)水平较治疗前均显著升高(P0.05),且观察组血清SOD、CAT、GSH-Px水平均明显比对照组高(P0.05)。两组治疗期间不良反应总发生率分别为10.64%(5/47)、4.26%(2/47),组间比较差异无统计学意义(P0.05)。结论:普罗布考联合胰激肽原酶治疗老年糖尿病周围神经病变患者的效果显著优于单用胰激肽原酶治疗,可更有效改善神经病变程度,其机制可能和缓解氧化应激反应、降低血清NSE水平有关。     

磁共振成像弥散张量成像参数联合血清NSE、Lp-PLA2在脑梗死患者的诊断和预后不良风险评估中的应用价值

摘要 目的：探讨磁共振成像（MRI）弥散张量成像（DTI）参数联合血清神经元特异性烯醇化酶（NSE）、脂蛋白相关磷脂酶A2（Lp-PLA2）在脑梗死患者的诊断和预后不良风险评估中的应用价值。方法：选择2021年3月至2022年9月吉林大学中日联谊医院收治的106例脑梗死患者作为脑梗死组，另选同期62例体检健康志愿者作为对照组，比较两组DTI参数，血清NSE和Lp-PLA2水平。脑梗死组出院90d后，采用改良Rankin量表（mRS）进行预后评估，分为预后良好组与预后不良组，并比较两组上述指标水平。受试者工作特征（ROC）曲线分析DTI参数联合血清NSE、Lp-PLA2诊断脑梗死和预测脑梗死患者预后的价值。结果：脑梗死组表观弥散系数（ADC）值、部分各向异性指数（FA）值低于对照组（P＜0.05），血清NSE、Lp-PLA2水平高于对照组（P＜0.05）。预后不良组FA值、ADC值低于预后良好组（P＜0.05），血清NSE、Lp-PLA2水平高于预后良好组（P＜0.05）。联合FA值、ADC值、NSE和Lp-PLA2诊断脑梗死以及预测脑梗死患者预后不良的曲线下面积（AUC）分别为0.852、0.874，均高于各因素单独诊断和预测。结论：脑梗死DTI参数FA值、ADC值降低，血清NSE、Lp-PLA2水平增高，联合DTI参数和血清NSE、Lp-PLA2检测在脑梗死诊断和预后预测中具有较高价值。     

Enolases from Gram-positive bacterial pathogens and commensal lactobacilli share functional similarity in virulence-associated traits

Enolase occurs as a cytoplasmic and a surface-associated protein in bacteria. Enolases of the bacterial pathogens Streptococcus pyogenes, Streptococcus pneumoniae and Staphylococcus aureus, as well as of the commensal lactic acid bacteria, Lactobacillus crispatus and Lactobacillus johnsonii, were purified as His(6)-fusion proteins from recombinant Escherichia coli. The fusion proteins were compared for putative virulence-associated functions, i.e., binding of human plasminogen, enhancement of plasminogen activation by human plasminogen activators, as well as binding to immobilized laminin, fibronectin and collagens. The individual enolases showed varying efficiencies in these functions. In particular, highly and equally effective interactions with plasminogen and laminin were seen with lactobacillar and staphylococcal enolases.     

Is 2-phosphoglycerate-dependent automodification of bacterial enolases implicated in their export?

We observed that in vivo and in vitro a small fraction of the glycolytic enzyme enolase became covalently modified by its substrate 2-phosphoglycerate (2-PG). In modified Escherichia coli enolase, 2-PG was bound to Lys341, which is located in the active site. An identical reversible modification was observed with other bacterial enolases, but also with enolase from Saccharomyces cerevisiae and rabbit muscle. An equivalent of Lys341, which plays an important role in catalysis, is present in enolase of all organisms. Covalent binding of 2-PG to this amino acid rendered the enzyme inactive. Replacement of Lys341 of E.coli enolase with other amino acids prevented the automodification and in most cases strongly reduced the activity. As reported for other bacteria, a significant fraction of E.coli enolase was found to be exported into the medium. Interestingly, all Lys341 substitutions prevented not only the automodification, but also the export of enolase. The K341E mutant enolase was almost as active as the wild-type enzyme and therefore allowed us to establish that the loss of enolase export correlates with the loss of modification and not the loss of glycolytic activity.     

Various tolerances to arsenic trioxide between human cortical neurons and leukemic cells

Arsenic trioxide (As2O3) is very effective for treatment of acute promyelocytic leukaemia (APL) but little can pass through the blood-brain-barrier (BBB),which limits its use in the prevention and treatment of central nervous system leukaemia (CNSL). Before creating a non-invasive method to help As2O3 ’s access,the safe and effective therapeutic concentration of As2O3 in the CNS ought to be known. The changes of apoptosis biomarkers,[Ca2 ]i and PKC activity of both leukaemia cells and human cortical neurons,were monitored before and after being treated with As2O3 in vitro with laser confocal microscopy and Western blot. NSE concentration,the neuron invasive biomarker,was monitored by enzyme immunoassay (NSE-EIA). This study revealed that cortical neuron was more tolerable to As2O3 compared to NB4. 1.0 μmol / L As2O3 showed little influence on cortical neuron but effectively promoted apoptosis and induced differentiation of NB4.     

Neurogenic differentiation of human adipose-derived stem cells: Relevance of different signaling molecules,transcription factors,and key marker genes

Since numerous diseases affect the central nervous system and it has limited self-repair capability, a great interest in using stem cells as an alternative cell source is generated. Previous reports have shown the differentiation of adipose-derived stem cells in neuron-like cells and it has also been proved that the expression pattern of patterning, proneural, and neural factors, such as Pax6, Mash1, Ngn2, NeuroD1, Tbr2 and Tbr1, regulates and defines adult neurogenesis. Regarding this, we hypothesize that a functional parallelism between adult neurogenesis and neuronal differentiation of human adipose-derived stem cells exists. In this study we differentiate human adipose-derived stem cells into neuron-like cells and analyze the expression pattern of different patterning, proneural, neural and neurotransmitter genes, before and after neuronal differentiation. The neuron-like cells expressed neuronal markers, patterning and proneural factors characteristics of intermediate stages of neuronal differentiation. Thus we demonstrated that it is possible to differentiate adipose-derived stem cells in vitro into immature neuron-like cells and that this process is regulated in a similar way to adult neurogenesis. This may contribute to elucidate molecular mechanisms involved in neuronal differentiation of adult human non-neural cells, in aid of the development of potential therapeutic tools for diseases of the nervous system.     

Sulfenylation of ENOLASE2 facilitates H2O2-conferred freezing tolerance in Arabidopsis

1. Download : Download high-res image (155KB)
2. Download : Download full-size image